Atherosclerosis is the underlying mechanism of ischemic heart disease and stroke, which represent the most common cause of death in the United States. Atherogenesis starts from the deposition of ApoB-containing lipoproteins, such as low-density lipoproteins and chylomicron remnants, in the intima of the arterial wall. Macrophages then take up the deposited lipoproteins and transform into foam cells1. The presence of foam cells in the arterial intima is a hallmark feature of atherosclerosis. Continued accumulation of lipid and lipid-laden foam cells, and the succeeded proliferation of smooth muscle and connective tissue give rise to atherosclerotic plaques. Rupture of a plaque triggers thrombosis and/or embolism that may cause luminal occlusion in coronary or cerebral arteries, resulting in heart attack and stroke1,2.